The pathogenesis of group B streptococci in lung tissue will be studied in vivo and in vitro using the mouse model of early onset disease of the human newborn. The interaction of virulent and avirulent strains of group B streptococci and/or their purified and characterized protease, hyaluronidase, and lipoteichoic acid with lung tissue will be measured quantitatively by their effects on the function of alveolar type I and type II epithelial cells and alveolar macrophages. The mechanism for the decrease in pulmonary surfactant and an alteration in the function of type II epithelial cells in infected mice will be discerned through changes in the specific activity of dipalmitoylphosphatidylcholine and its redistribution in the separated fractions of lung tissue. Alteration in the permeability of the airblood barrier and type I cell function will be observed by the passage of intravenous 125I labeled albumin into the air spaces. Virulent and avirulent streptotoccoi and their components will be evaluated for their effects on the phagocytosis, killing, and acid hydrolase release functions of alveolar macrophages. The hypothesis that lipoteicholic acid by its interaction with surfactant lipid is required as a carrier for the mediation of pathogenesis by streptococcal hydrolytic enzymes will be tested.